The contact area between NAx-E2 mutant female germline stem cells and the niche is smaller than in wild type controls.
NAx-E2 mutant female germline stem cell (GSC) clones are lost more rapidly from the niche than their neighbouring control GSCs.
Heterozygotes show a loss of wing veins.
NAx-E2 mutants exhibit a loss of the fourth and fifth wing veins in male flies caused by a gain of function of Notch.
Heterozygotes have a gap at the distal end of wing vein L5.
Mutants have shortened L4 and L5 wing veins.
A small percentage of NAx-9/NAx-E2 flies survive to adulthood.
Mutant flies have 90.88 +/- 1.94 thoracic microchaetae per heminotum (compared to the wild-type number of 130.35 +/- 1.54).
Heterozygotes show loss of wing vein, with a penetrance of 8.7%.
NAx-E2 mutants exhibit elevated levels of asymmetry and reduced mean character size relative to Canton-S flies for thoracic bristles.
NAx-E2 mutants show significantly reduced mean character size for orbital bristles compared to Canton-S flies.
The number of missing bristles remains roughly equal with increasing temperature in homozygous flies, while the number and length of wing vein breaks increases with increasing temperature.
Some macrochaetae on the thorax are missing. Gaps in wing veins are present.
Abruptex wing phenotype dominantly enhanced by Su(H)2. Su(H)16 dominantly suppresses the lethality of NAx-E2/NAx-9 transheterozygotes.
Length of microchaetae, macrochaetae and longitudinal wing veins is reduced with respect to that of wild type. Enhances the N haplo-insufficient phenotype of loss of the wing margin. Heteroallelic combinations with lethal Abruptex alleles show stronger phenotypes at 29oC than when heterozygous with a N null at 29oC.
Short wing veins IV and V.
Heterozygotes with Dlsup4 and Dlsup5 exhibit shortening and fragmenting of vein IV only. Wing phenotype is enhanced by mutations at da.
Some hemizygous males occasionally lack the twin sensilla of the wing margin, the ventral sensillum of wing vein L3, and the anterior cross vein sensillum.
Homozygotes exhibit wing vein defects. Wing phenotype in unaffected by vg and sca mutations but enhanced when combined with deficiencies of vg and sca or just vg (wing scalloping and increased venation defects).
Mutant phenotype of transheterozygotes can be rescued when in combination with dxENU homozygotes. Male hemizygotes with dxENU have a low fertility and with dxS1M they are sterile.
Viable, enhancer type. NAx-E2/NAx-9 heterozygotes are lethal.
homozygous viable phenotype like NAx-1. Temperature sensitive for morphological phenotypes (Foster, 1975) but stable for viability (Portin and Siren, 1976). Viable in heterozygotes with N; Notch-wing phenotype is enhanced. At 18oC and 25oC, complementary in heterozygotes with recessive alleles at Notch; at 29oC, spl and Nnd-2 are weakly expressed (Portin, 1977a). Heterozygotes Nnd-3 spl NAx-E2/+++ are like spl/spl with suppression of wing-vein gaps; Nnd-3++/+ spl NAx-E2 and +spl NAx-E2/+++ show mild expression of spl (Foster, 1975). NAx-E2 is viable with alleles NAx-71d and NAx-16; lethal with lethal alleles NAx-59b and NAx-59d and with NAx-E1, NAx-9, and NAx-1 (Foster, 1975; Portin, 1975) and the lethality with NAx-1 is more pronounced at 29oC (Portin and Siren, 1976). In NAx-E2/NAx-1, the TSP for lethality is monophasic from the end of the third instar to early pupa (Portin and Siren, 1976). In NAx-E2/NAx-9, the focus of lethality is close to hypodermal sites of ventral thoracic structures, and in surviving gynandromorphs, the negative interaction between alleles is autonomous (Portin, 1977). NAx-E2 is placed on the genetic map of Notch close to and to the right of spl (Foster).